madman
Super Moderator
Abstract
Insulin resistance is a key feature of Type 2 diabetes and an important therapeutic target to address glycemic control to prevent diabetic complications. Lifestyle advice is the first step in the ADA/EASD consensus guidelines followed by metformin therapy. Aerobic exercise (AE) can increase insulin sensitivity by several molecular pathways including upregulation of insulin transporters in the cellular membrane of insulin‐dependent cells. In addition, AE improves insulin sensitivity by amelioration of the pathophysiologic pathways involved in insulin resistance such as the reduction of adipokines, inflammatory and oxidative stress responses, and improvement of insulin signal transduction via different molecular pathways. This review details the molecular pathways by which AE induces beneficial effects on insulin resistance
5 | CONCLUSION
The available data suggest that AE increases insulin sensitivity in peripheral tissues, leading to improved glucose homeostasis and a reduction in insulin resistance through at least seven different molecular mechanisms (Figure 1). AE can upregulate GLUT‐4 and increase its density in insulin‐dependent cell membranes; additionally, AE may also improve insulin sensitivity by a reduction in adipokines; AE improves oxidative stress‐induced insulin resistance by normalizing the redox state. In addition, improvement of β cell function, modulation of IRS‐1 phosphorylation, lowering of ceramide plasma levels, and induction of angiogenesis are other molecular mechanisms by which AE improves IST leading to increased insulin sensitivity and enhanced glucose metabolism that may lead to a lower incidence of diabetic complications plus other metabolic and nonmetabolic effects (Figure 2).
Insulin resistance is a key feature of Type 2 diabetes and an important therapeutic target to address glycemic control to prevent diabetic complications. Lifestyle advice is the first step in the ADA/EASD consensus guidelines followed by metformin therapy. Aerobic exercise (AE) can increase insulin sensitivity by several molecular pathways including upregulation of insulin transporters in the cellular membrane of insulin‐dependent cells. In addition, AE improves insulin sensitivity by amelioration of the pathophysiologic pathways involved in insulin resistance such as the reduction of adipokines, inflammatory and oxidative stress responses, and improvement of insulin signal transduction via different molecular pathways. This review details the molecular pathways by which AE induces beneficial effects on insulin resistance
5 | CONCLUSION
The available data suggest that AE increases insulin sensitivity in peripheral tissues, leading to improved glucose homeostasis and a reduction in insulin resistance through at least seven different molecular mechanisms (Figure 1). AE can upregulate GLUT‐4 and increase its density in insulin‐dependent cell membranes; additionally, AE may also improve insulin sensitivity by a reduction in adipokines; AE improves oxidative stress‐induced insulin resistance by normalizing the redox state. In addition, improvement of β cell function, modulation of IRS‐1 phosphorylation, lowering of ceramide plasma levels, and induction of angiogenesis are other molecular mechanisms by which AE improves IST leading to increased insulin sensitivity and enhanced glucose metabolism that may lead to a lower incidence of diabetic complications plus other metabolic and nonmetabolic effects (Figure 2).
